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Transverse myelitis
Dr Suraj B.Kanase
Associate professor
Dep of Neurophysiotherapy
Krishna Institute Of Medical Sciences Deemed To Be University
Learning objectives
1. Introduction to transverse myelits
2. Pathophysiology.
3. Signs and symptoms.
4. Diagnostic criteria
5. Invetigations
6. Aims of physiotherapy management
7. Means of management.
• Transverse myelitis (TM) is a rare neurological condition in which
the spinal cord is inflamed. Transverse implies that the inflammation
extends horizontally across the spinal cord.
• Partial transverse myelitis and partial myelitis are terms sometimes
used to specify inflammation that only affects part of the width of the
spinal cord.
Etiology :
• It is post infectious disorder of the spinal cord that is seen folowing an
episode of infleunza, mumps, measles or infectious caused by epstein barr
virus.
Pathophysiology :
• It is not a result of direct effect of virus on the spinal cord but is an
autoimmune response of the body whichgets provoked by infection.
• The lesions present are usually inflammatory. Spinal cord involvement is
usually central, uniform and symmetric in comparison to multiple sclerosis
which typically affects the cord in a patchy way and the lesions are usually
peripheral
• There is affection of white as well as gray matter. The spinal cord
appears edematous, hyperemic and infiltrated by inflammatory cells.
Signs and symptoms :
• The onset is usually acute or subacute.
• Disease usually starts either at back or neck area and is usually
localized.
• The spine becomes very tender around the affected area.
Sensory loss :
• The person may have altered sensations like paresthesia or loss of
sensation which begins in the distal part of the leg and ascends
upwards similar to one in GBS.
• However unlike GBS, there is a sensory level , elow which there is
complete loss of sensation and above the lesion there is normal
sensation.
• Between this normal and abnormal zone there may be a zone of
hypersensitivity in some patients.
Motor loss :
• Symptoms are similar to that of acute traumatic paraplegia with a
stage of spinal shock during which tone is lost and there is areflexia
but after some days of shock the tone gradually begins to build up and
the reflexes reappear. Babinski sign also becomes positive at this
stage.
• In case babinski sign fails to become positive then it indicates
necrosis involving multiple segments.
Sphincter disturbances :
• During the stage of spinal shock there is atonic bladder but after the
stage of spinal shock the patient has automatic bladder if the lesion is
above the spinal reflex center for micturition.
Segment wise symptoms
• If the upper cervical segment of the spinal cord is involved, all four
limbs may be affected and there is risk of respiratory failure – the
phrenic nerve which is formed by the cervical spinal nerves C3, C4,
and C5 innervates the main muscle of respiration, the diaphragm.
• Lesions of the lower cervical region (C5–T1) will cause a
combination of upper and lower motor neuron signs in the upper
limbs, and exclusively upper motor neuron signs in the lower limbs.
Cervical lesions account for about 20% of cases.
• A lesion of the thoracic segment (T1–12) will produce upper motor
neuron signs in the lower limbs, presenting as a spastic paraparesis.
This is the most common location of the lesion, and therefore most
individuals will have weakness of the lower limbs.
• A lesion of the lumbar segment, the lower part of the spinal cord
(L1–S5) often produces a combination of upper and lower motor
neuron signs in the lower limbs. Lumbar lesions account for about
10% of cases.
Diagnosis :
Diagnostic criteria
In 2002, the Transverse Myelitis Consortium Working Group proposed
the following diagnostic criteria for idiopathic acute transverse myelitis :
Inclusion criteria
• Motor, sensory or autonomic dysfunction attributable to spinal cord
• Signs and symptoms on both sides of the body (not necessarily
symmetrical)
• Clearly defined sensory level
• Signs of inflammation (pleocytosis of the cerebrospinal fluid, or
elevated immunoglobulin G, or evidence of inflammation on
gadolinium-enhanced (MRI) Magnetic resonance imaging)
• Peak of this condition can occur anytime between 4 hours to 21 days
after onset
Exclusion criteria
• Irradiation of the spine (e.g., radiotherapy) in the last 10 years
• Evidence of thrombosis of the anterior spinal artery
• Evidence of extra-axial compression on neuroimaging
• Evidence of arteriovenous malformation (abnormal flow voids on
surface of spine)
• Evidence of connective tissue disease, e.g. sarcoidosis, Behçet's
disease, Sjögren's syndrome, systemic lupus erythematosus or mixed
connective tissue disease
• Evidence of optic neuritis (diagnostic of neuromyelitis optica)
• Evidence of infection (syphilis, Lyme disease, Human
immunodeficiency virus, Human T-lymphotropic virus 1,
mycoplasma, Herpes simplex virus, Varicella-zoster virus, Epstein-
Barr virus, cytomegalovirus, Human herpesvirus 6 or enteroviruses)
• Evidence of multiple sclerosis (abnormalities detected on MRI and
presence of oligoclonal antibodies in cerebrospinal fluid (CSF))
Investigations :
• Individuals who develop TM are typically transferred to a neurologist or
neurosurgeon who can urgently investigate the patient in a hospital.
• If breathing is affected, particularly in upper spinal cord lesions, methods
of artificial ventilation must be on hand before and during the transfer
procedure.
• The patient should also be catheterized to test for and, if necessary, drain
an over-distended bladder. A lumbar puncture can be performed after the
MRI or at the time of CT myelography.
• Corticosteroids are often given in high doses when symptoms begin with
the hope that the degree of inflammation and swelling of the spinal cord
will be lessened, but whether this is truly effective is still debated
Differential diagnosis :
The differential diagnosis of acute TM includes
• Demyelinating disorders, such as multiple sclerosis and neuromyelitis
optica,
• Infections, such as herpes zoster and herpes simplex virus, and
• Other types of inflammatory disorders, such as systemic lupus
erythematosus and neurosarcoidosis.
• It is important to also rule out an acute cause of compression on the
spinal cord.
Aims of physiotherapy
The aims of physiotherapy can be:
• To increase quality of life
• To increase independence
• To increase muscle strength
• To increase energy levels
• To reduce pain and muscle spasms
• To reduce stiffness
• To reduce risk of chest infections
Physiotherapy Treatment :
1. Counselling
2. Maintaining passive and active range of motion
3. Maintenance of good bronchial hygiene
4. Care of skin
5. Care of bladder
6. Active exercises
7. Management of spasticity
8. Mat exercises
• Strengthening exercises
• Use of titlt table
• Transfer activites
• Gait training
• Social and econimocal rehabilitation.
THANK YOU

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Transverse myelitis

  • 1. Transverse myelitis Dr Suraj B.Kanase Associate professor Dep of Neurophysiotherapy Krishna Institute Of Medical Sciences Deemed To Be University
  • 2. Learning objectives 1. Introduction to transverse myelits 2. Pathophysiology. 3. Signs and symptoms. 4. Diagnostic criteria 5. Invetigations 6. Aims of physiotherapy management 7. Means of management.
  • 3.
  • 4. • Transverse myelitis (TM) is a rare neurological condition in which the spinal cord is inflamed. Transverse implies that the inflammation extends horizontally across the spinal cord. • Partial transverse myelitis and partial myelitis are terms sometimes used to specify inflammation that only affects part of the width of the spinal cord.
  • 6. • It is post infectious disorder of the spinal cord that is seen folowing an episode of infleunza, mumps, measles or infectious caused by epstein barr virus. Pathophysiology : • It is not a result of direct effect of virus on the spinal cord but is an autoimmune response of the body whichgets provoked by infection. • The lesions present are usually inflammatory. Spinal cord involvement is usually central, uniform and symmetric in comparison to multiple sclerosis which typically affects the cord in a patchy way and the lesions are usually peripheral
  • 7. • There is affection of white as well as gray matter. The spinal cord appears edematous, hyperemic and infiltrated by inflammatory cells. Signs and symptoms : • The onset is usually acute or subacute. • Disease usually starts either at back or neck area and is usually localized. • The spine becomes very tender around the affected area.
  • 8. Sensory loss : • The person may have altered sensations like paresthesia or loss of sensation which begins in the distal part of the leg and ascends upwards similar to one in GBS. • However unlike GBS, there is a sensory level , elow which there is complete loss of sensation and above the lesion there is normal sensation.
  • 9. • Between this normal and abnormal zone there may be a zone of hypersensitivity in some patients. Motor loss : • Symptoms are similar to that of acute traumatic paraplegia with a stage of spinal shock during which tone is lost and there is areflexia but after some days of shock the tone gradually begins to build up and the reflexes reappear. Babinski sign also becomes positive at this stage.
  • 10. • In case babinski sign fails to become positive then it indicates necrosis involving multiple segments. Sphincter disturbances : • During the stage of spinal shock there is atonic bladder but after the stage of spinal shock the patient has automatic bladder if the lesion is above the spinal reflex center for micturition.
  • 11. Segment wise symptoms • If the upper cervical segment of the spinal cord is involved, all four limbs may be affected and there is risk of respiratory failure – the phrenic nerve which is formed by the cervical spinal nerves C3, C4, and C5 innervates the main muscle of respiration, the diaphragm. • Lesions of the lower cervical region (C5–T1) will cause a combination of upper and lower motor neuron signs in the upper limbs, and exclusively upper motor neuron signs in the lower limbs. Cervical lesions account for about 20% of cases.
  • 12. • A lesion of the thoracic segment (T1–12) will produce upper motor neuron signs in the lower limbs, presenting as a spastic paraparesis. This is the most common location of the lesion, and therefore most individuals will have weakness of the lower limbs. • A lesion of the lumbar segment, the lower part of the spinal cord (L1–S5) often produces a combination of upper and lower motor neuron signs in the lower limbs. Lumbar lesions account for about 10% of cases.
  • 13. Diagnosis : Diagnostic criteria In 2002, the Transverse Myelitis Consortium Working Group proposed the following diagnostic criteria for idiopathic acute transverse myelitis : Inclusion criteria • Motor, sensory or autonomic dysfunction attributable to spinal cord • Signs and symptoms on both sides of the body (not necessarily symmetrical) • Clearly defined sensory level
  • 14. • Signs of inflammation (pleocytosis of the cerebrospinal fluid, or elevated immunoglobulin G, or evidence of inflammation on gadolinium-enhanced (MRI) Magnetic resonance imaging) • Peak of this condition can occur anytime between 4 hours to 21 days after onset Exclusion criteria • Irradiation of the spine (e.g., radiotherapy) in the last 10 years • Evidence of thrombosis of the anterior spinal artery
  • 15. • Evidence of extra-axial compression on neuroimaging • Evidence of arteriovenous malformation (abnormal flow voids on surface of spine) • Evidence of connective tissue disease, e.g. sarcoidosis, Behçet's disease, Sjögren's syndrome, systemic lupus erythematosus or mixed connective tissue disease • Evidence of optic neuritis (diagnostic of neuromyelitis optica)
  • 16. • Evidence of infection (syphilis, Lyme disease, Human immunodeficiency virus, Human T-lymphotropic virus 1, mycoplasma, Herpes simplex virus, Varicella-zoster virus, Epstein- Barr virus, cytomegalovirus, Human herpesvirus 6 or enteroviruses) • Evidence of multiple sclerosis (abnormalities detected on MRI and presence of oligoclonal antibodies in cerebrospinal fluid (CSF))
  • 17. Investigations : • Individuals who develop TM are typically transferred to a neurologist or neurosurgeon who can urgently investigate the patient in a hospital. • If breathing is affected, particularly in upper spinal cord lesions, methods of artificial ventilation must be on hand before and during the transfer procedure. • The patient should also be catheterized to test for and, if necessary, drain an over-distended bladder. A lumbar puncture can be performed after the MRI or at the time of CT myelography. • Corticosteroids are often given in high doses when symptoms begin with the hope that the degree of inflammation and swelling of the spinal cord will be lessened, but whether this is truly effective is still debated
  • 18. Differential diagnosis : The differential diagnosis of acute TM includes • Demyelinating disorders, such as multiple sclerosis and neuromyelitis optica, • Infections, such as herpes zoster and herpes simplex virus, and • Other types of inflammatory disorders, such as systemic lupus erythematosus and neurosarcoidosis. • It is important to also rule out an acute cause of compression on the spinal cord.
  • 19. Aims of physiotherapy The aims of physiotherapy can be: • To increase quality of life • To increase independence • To increase muscle strength • To increase energy levels • To reduce pain and muscle spasms • To reduce stiffness • To reduce risk of chest infections
  • 20. Physiotherapy Treatment : 1. Counselling 2. Maintaining passive and active range of motion 3. Maintenance of good bronchial hygiene 4. Care of skin 5. Care of bladder 6. Active exercises 7. Management of spasticity 8. Mat exercises
  • 21. • Strengthening exercises • Use of titlt table • Transfer activites • Gait training • Social and econimocal rehabilitation.